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Cat. No. ARG37598

HOXB5 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

This product is a CRISPR/Cas9-edited polyclonal HOXB5 knockout cell population derived from the HeLa cervical adenocarcinoma cell line. HOXB5, a homeobox transcription factor, regulates anterior-posterior patterning and hematopoietic development and is implicated in retinoic acid, Wnt, BMP, and FGF signaling pathways. Loss of HOXB5 disrupts transcriptional control of proliferation and adhesion targets, with interacting cofactors such as PBX and MEIS. These cells are suited for cancer biology studies, drug screening, and developmental research using assays like RNA-seq, western blot, and migration assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    HOXB5

    Gene Identifier

    NCBI Gene ID 3215

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The HOXB5 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa parental line, designed for targeted disruption of the HOXB5 gene. The knockout approach abrogates HOXB5 transcriptional activity, enabling researchers to study the gene’s role in cellular processes without clone-specific artifacts. This format is ideal for experiments requiring population-level analysis and consistent knockout effects across assays.

The HeLa host cell line is an epithelial adenocarcinoma line originally derived from a cervical cancer biopsy and is positive for human papillomavirus type 18 (HPV-18). Widely utilized in biomedical research, HeLa cells exhibit rapid proliferation and high transfectability, making them a versatile platform for genetic manipulation and functional genomics studies. Their well-characterized genome and ease of culture facilitate reproducible experimental outcomes. In the context of HOXB5 knockout, HeLa cells provide a relevant epithelial cancer model to investigate the transcription factor’s contributions to oncogenesis and cellular differentiation.

HOXB5 encodes a homeobox transcription factor that regulates anterior-posterior patterning during development and plays roles in hematopoietic differentiation. Mechanistically, HOXB5 is activated by retinoic acid signaling through RAR/RXR heterodimers and by Wnt/??-catenin/TCF pathways, while also receiving inputs from BMP/SMAD1/5/8 and FGF receptor cascades. HOXB5 interacts with PBX and MEIS cofactors to form transcriptional complexes that modulate the expression of downstream targets, including cell adhesion molecules, cell cycle regulators, and other developmental transcription factors. Disruption of HOXB5 in HeLa cells uncouples these signaling networks, leading to altered proliferation, adhesion, and differentiation programs.

In the HeLa cervical adenocarcinoma background, loss of HOXB5 disrupts its oncogenic transcriptional programs, offering insight into the molecular mechanisms underlying tumor growth and metastasis. Given HOXB5??s involvement in acute myeloid leukemia and breast cancer, these cells serve as a cross-tissue model for studying conserved HOX-dependent pathways in cancer. The polyclonal nature ensures that observed phenotypes are representative of heterogeneous knockout outcomes, reflecting real-world tumor heterogeneity. Consequently, this model is valuable for validating HOXB5 as a therapeutic target and for screening compounds that may modulate HOXB5-mediated signaling or compensate for its loss.

Typical research applications include gene function studies through RT-qPCR and western blot analysis of HOXB5 target genes, proliferation and migration/invasion assays to assess oncogenic phenotypes, and global expression profiling via RNA-seq. Immunofluorescence can be used to examine changes in cell adhesion and cytoskeletal organization. The cells are also suitable for drug target screening to identify small molecules that inhibit proliferation or restore differentiation in HOXB5-deficient contexts. For further details, technical support, or custom orders, please contact Ascent Research.

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